Abstract
Epilepsy is one of the most common neurological diseases, and seizures cannot be controlled in 30% of patients. Therefore, the development of new pharmacological approaches is required. In some pharmacoresistant forms of epilepsy, the mechanisms for the glutamate removal from the synaptic cleft may be disrupted. Therefore, one of the promising approaches for such pathological conditions in an increase of functional activity of glutamate transporters. In this review, we analyze current data on changes in the expression of excitatory amino acid transporters (EAAT) in human epilepsy, as well as in animal models of seizures and epilepsy. The pharmacological approaches that change the expression and activity of EAATs are considered. The special attention is paid to the analysis of the use of the antibiotic ceftriaxone, which enhances the expression and activity of EAAT-2.
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